The study shows that a tiny protein called Humanin, made from a mitochondrial gene, can protect brain cells from damage linked to Alzheimer’s disease, but it might also raise the chance of developing cancer, so its use is risky and not ready for everyday self‑experimentation.

New functions of well-known genes have been revealed frequently. A new example is described in this report. Earlier we have detected an up-regulation of expression of the mitochondrial 16S rRNA gene in non-Hodgkin's lymphomas. Here we demonstrate that the human mitochondrial 16S rRNA gene encodes a potential oncopeptide, Humanin described recently. This peptide suppresses neuronal cell death induced by mutant genes responsible for familial Alzheimer's disease (AD). Analysis of the gene coding site structure showed that Humanin mRNA is translated most likely in the cytosol, but not in the mitochondrion in vivo. This led us to suppose that AD could be caused by a block of Humanin mRNA transport from mitochondria into the cytosol. Moreover, our data and reports by others an mitochondrial 16S rRNA transcription and characteristic of transcript structure suggests that Humanin is a potential oncopeptide. Thus, the use of Humanin for the treatment of AD may increase the risk for the development of malignant diseases.